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终末期特发性和缺血性心肌病中的HLA抗原频率。

HLA antigen frequencies in end-stage idiopathic and ischaemic cardiomyopathy.

作者信息

Harcombe A A, Sharples L, Large S R, Wallwork J, Weissberg P L, Joysey V

机构信息

Transplant Unit, Papworth Hospital NHS Trust, Cambridge, UK.

出版信息

Int J Cardiol. 1999 Jan;68(1):31-7. doi: 10.1016/s0167-5273(98)00336-2.

DOI:10.1016/s0167-5273(98)00336-2
PMID:10077398
Abstract

We investigated the distribution of HLA antigens among 413 patients with ischaemic heart disease or dilated cardiomyopathy referred for cardiac transplantation to determine if possession of certain HLA antigens predisposed to end-stage heart failure. Of the patients studied, 234 had ischaemic heart disease (218 males), mean age 49 years (SD 7.1) and 179 patients had dilated cardiomyopathy (150 males), mean age 39 years (12.8). The control group comprised 2041 kidney donors reported to the United Kingdom Transplant Service between July and August 1985. We found a significant excess of HLA DR1 (odds ratio 1.64, 95% CI 1.16-2.33, attributable risk 5.0%) and DR5 antigens (odds ratio 1.47, 95% CI 0.99-2.18, attributable risk) among patients with dilated cardiomyopathy but not of HLA DR4 as previously reported. We found a lower frequency than expected of HLA B21 (10.44 expected, none observed) among patients with ischaemic heart disease but no other significant differences. This study provides some support for the concept of the risk of developing end-stage heart failure due to dilated cardiomyopathy being associated with possession of HLA DR1 and DR5, but no such evidence in ischaemic heart disease. Larger multi-centre studies are required to confirm the validity of these findings.

摘要

我们调查了413例因缺血性心脏病或扩张型心肌病而转诊接受心脏移植的患者中HLA抗原的分布情况,以确定某些HLA抗原的携带是否易导致终末期心力衰竭。在研究的患者中,234例患有缺血性心脏病(218例男性),平均年龄49岁(标准差7.1),179例患者患有扩张型心肌病(150例男性),平均年龄39岁(12.8)。对照组包括1985年7月至8月间向英国移植服务机构报告的2041名肾脏供体。我们发现扩张型心肌病患者中HLA DR1抗原显著过多(优势比1.64,95%可信区间1.16 - 2.33,归因风险5.0%)以及DR5抗原(优势比1.47,95%可信区间0.99 - 2.18,归因风险),但未发现如先前报道的HLA DR4抗原过多情况。我们发现缺血性心脏病患者中HLA B21抗原的频率低于预期(预期为10.44,未观察到),但无其他显著差异。本研究为扩张型心肌病导致终末期心力衰竭的风险与HLA DR1和DR5的携带相关这一概念提供了一些支持,但在缺血性心脏病中未发现此类证据。需要更大规模的多中心研究来证实这些发现的有效性。

相似文献

1
HLA antigen frequencies in end-stage idiopathic and ischaemic cardiomyopathy.终末期特发性和缺血性心肌病中的HLA抗原频率。
Int J Cardiol. 1999 Jan;68(1):31-7. doi: 10.1016/s0167-5273(98)00336-2.
2
HLA-DR antigen linkage of anti-beta receptor antibodies in idiopathic dilated and ischaemic cardiomyopathy.特发性扩张型和缺血性心肌病中抗β受体抗体与HLA - DR抗原的关联
Br Heart J. 1992 May;67(5):402-5. doi: 10.1136/hrt.67.5.402.
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Do specific HLA antigens predispose to ischaemic heart disease or idiopathic dilated cardiomyopathy?特定的人类白细胞抗原(HLA)抗原是否易患缺血性心脏病或特发性扩张型心肌病?
Br Heart J. 1994 Jan;71(1):76-8. doi: 10.1136/hrt.71.1.76.
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HLA antigens in idiopathic dilated cardiomyopathy.特发性扩张型心肌病中的人类白细胞抗原
Br Heart J. 1989 Nov;62(5):379-83. doi: 10.1136/hrt.62.5.379.
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Antigens of the major histocompatibility system in ischemic heart disease and idiopathic dilated cardiomyopathy.缺血性心脏病和特发性扩张型心肌病中主要组织相容性系统的抗原
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Anti-beta-receptor antibodies in human dilated cardiomyopathy and correlation with HLA-DR antigens.人类扩张型心肌病中的抗β受体抗体及其与HLA-DR抗原的相关性
Am J Cardiol. 1990 Feb 15;65(7):483-7. doi: 10.1016/0002-9149(90)90815-i.
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Influence of anti-beta-receptor antibodies on cardiac adenylate cyclase in patients with idiopathic dilated cardiomyopathy.抗β受体抗体对特发性扩张型心肌病患者心脏腺苷酸环化酶的影响。
Am Heart J. 1990 Jun;119(6):1322-8. doi: 10.1016/s0002-8703(05)80182-6.
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Idiopathic dilated cardiomyopathy: lack of association between circulating organ-specific cardiac antibodies and HLA-DR antigens.特发性扩张型心肌病:循环器官特异性心脏抗体与HLA - DR抗原之间缺乏关联。
Tissue Antigens. 1992 May;39(5):236-40. doi: 10.1111/j.1399-0039.1992.tb01941.x.
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HLA A, B and DR typing in idiopathic dilated cardiomyopathy: a search for immune response factors.特发性扩张型心肌病中的HLA A、B及DR分型:寻找免疫反应因子
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[HLA A-B and DR in dilated myocardiopathies].[扩张型心肌病中的人类白细胞抗原A-B和DR]
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2
A meta-analysis of HLA-DR polymorphism and genetic susceptibility to idiopathic dilated cardiomyopathy.HLA-DR 多态性与特发性扩张型心肌病遗传易感性的荟萃分析。
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Autoimmune cardiomyopathy and heart block develop spontaneously in HLA-DQ8 transgenic IAbeta knockout NOD mice.
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